Familial clustering of vitamin D deficiency via shared environment: The Korean National Health and Nutrition Examination Survey 2008-2012.
Eur J Clin Nutr. 2018 Dec;72(12):1700-1708. doi: 10.1038/s41430-018-0157-3. Epub 2018 Apr 18.
>10,000 Korean families Deficiency : < 12 ng
Some reasons to believe the results of this study
- Poor responses to UV and Vitamin D were correlated to just 4 poor genes – June 2019
- 10 reasons for poor response to Vitamin D (race, binding protein, etc.) – Nov 2017
- Infant 7.6 X more likely to be Vitamin D deficient if mother had been – Nov 2019
- All family members had darker skin, and thus get less vitamin D from the sun
- All family members had daker skin and also wanted to have lighter skin - and those avoid the sun
- All family members avoid eating oily fish - thus get less vitamin D from food
- All members of the family are overweight - which reduces blood level of vitamin D
Download the PDF from VitaminDWiki
Hong N1,2, Lee YK1, Rhee Y3.
1 Department of Internal Medicine, Severance Hospital, Endocrine Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, Republic of Korea.
2 Graduate School, Yonsei University College of Medicine, Seoul, Republic of Korea.
3 Department of Internal Medicine, Severance Hospital, Endocrine Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, Republic of Korea. yumie at yuhs.ac.
BACKGROUND/OBJECTIVES:
Familial correlation of serum 25-hydroxyvitamin D concentration (25(OH)D) was reported in twin- or parent-offspring studies. However, data on relative contribution of environmental factors on familial clustering of 25(OH)D in extended families are limited.
SUBJECTS/METHODS:
We performed cross-sectional study using data from the Korean National Health and Nutrition Examination Survey (KNHANES) 2008-2012. Familial correlations of 25(OH)D were estimated in 28,551 subjects from 10,882 families. The variance component method was used to assess the relative contribution of additive genetic or environmental contributions to the variation in 25(OH)D level. Logistic regression models with interaction term were built to evaluate the differential influence of parental vitamin D status on the adolescents and adults offspring.
RESULTS:
Mean serum 25(OH)D concentration of subjects was 44.6 nmol/L (vitamin D insufficiency (30-50 nmol/L), 51%; vitamin D deficiency ( < 30 nmol/L), 17%). Familial clustering explained 40% of the total variation in 25(OH)D. In the variance component model, 4%, 39%, and 57% of the variation in serum 25(OH)D level was attributed to additive genetic, common shared environmental, and individual environmental factors, respectively. The odds of vitamin D deficiency in offspring with both parents with vitamin D deficiency compared with those with both parents with sufficient vitamin D levels was greater in adolescents ( < 19 years) than in adults ( ≥ 19 years) (odds ratio = 41.1 vs. 12.5; p for interaction = 0.03).
CONCLUSIONS:
We found a familial clustering of vitamin D deficiency in a large family-based cohort. Parental influence on vitamin D status of offspring was greater in adolescents than in adults.